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OPTOM 8060 BIOCHEM Midterm 2 > Lipid metabolism > Flashcards

Lipid metabolism Flashcards

1
Q

triglycerides

A

-triglycerides are storage molecules for lipids
-water insoluble
- no risk of undesired breakage

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2
Q

triglyceride transport

A
  • ingested triglycerides need a protein carrier to travel through the blood, to make them overall water soluble
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3
Q

triglyceride breakdown

A
  • uses coenzyme A to breakdown triglycerides to be used for fuel
  • beta-oxidation
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4
Q

how are fatty acid fuels obtained (3 ways)

A
  1. fats consumed in diet
  2. fats stored in cells as lipid droplets
  3. synthesis of fats by the liver
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5
Q

bile salts definition

A
  • synthesized molecules from cholesterol in the liver, stored in the gallbladder, and released into the small intestine after ingestion of fatty meal
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6
Q

bile salts role in triglyceride breakdown

A
  • solubilizes triglycerides by creating a mixed micelle of bile salts and triacylglycerol (aka triglyceride)
  • aids in lipid breakdown/ and absorption of digested products
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7
Q

what happens after bile salts interaction?

A
  • micelle is able to interact with water-soluble pancreatic lipase in the intestine
  • which breaks triglycerides to smaller pieces (mono/diglycerides, free FA)
  • these products dissolve into intestinal mucosa and are then reconverted into triacylglycerol packaged into chylomicrons in the ER
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8
Q

chylomicron structure

A
  • triacylglycerol in the center, with protein, phospholipids and cholesterol on the outside
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9
Q

what is an apolipoprotein

A

lipid-binding protein in the blood

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10
Q

what is a lipoprotein

A

combination of a lipid and an apolipoprotein

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11
Q

what is a chylomicron

A
  • largest type of lipoprotein and least dense
  • it’s synthesized in the epithelial cells of the small intestine, and transported via lymphatic tissue into the bloodstream
  • delivers dietary triglycerides to various tissue
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12
Q

what important apolipoprotein does chylomicrons contain and what do they do?

A

ApoC-II, important because it activate lipoprotein lipase which allows triglycerides to breakdown into FA’s in tissues

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13
Q

what happens to chylomicron remnants after chylomicrons are broken down?

A

Re-circulated into the liver, cholesterol is released and remainder is degraded into lysosomes in the hepatocytes

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14
Q

VLDL (very low-density lipoproteins)

A
  • happens when intake of FA’s is more than what’s need immediately for fuel:
  • then is converted to triacylglycerol in the liver and packaged as VLDL
  • transported to muscle for energy or adipose tissue for storage of lipid droplets
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15
Q

LPL (lipoprotein lipase)

A

enzyme that breaks down chylomicrons and VLDL from triglycerides to FA’s, different function based on tissue
- cardiac and skeletal muscle: provides energy
- adipose tissue: stimulates triacylglycerol storage

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16
Q

LPL in high vs low insulin levels

A
  • high insulin: increase of LPL in adipose tissue = fuel storage
  • low insulin: increase LPL activity in muscle tissue, release FA’s from VLDL for fuel
17
Q

IDL (intermediate-density lipoprotein)

A
  • these are equivalent to VLDL remnants
  • either are removed from the bloodstream by the liver or a precursor for LDL’s
18
Q

LDL (low-density lipoproteins)

A

-uses apolipoprotein ApoB-100 to transport to target tissue
- transports cholesterol to tissues, cholesterol uptake into extrahepatic tissues

19
Q

HDL (high-density lipoprotein)

A
  • contains enzyme cholesterol acyl transferase (LCAT)
  • catalyzes the formation of cholesteryl esters
  • extract cholesterol from chylomicrons and VLDL remnants
20
Q

why is HDL transportation unique

A

it’s reversal cholesterol transport, which means it picks up cholesterol in the tissues and carries it to the liver

21
Q

what organ is capable of disposing of significant amounts of cholesterol

A

the liver

22
Q

Acyl-CoA: cholesterol acyltransferase (ACAT)

A

esterifies free cholesterol by linking it to a fatty acid, preparing it for storage in liver cells or packaging into lipoproteins

23
Q

LDL - lipid transport

A
  • distribution and delivery of cholesterol to peripheral tissues is mediated by binding of LDL to LDL receptors on plasma membrane of target cells
24
Q

LDL receptors relation to high intracellular cholesterol

A
  • high intracellular cholesterol reduces LDL receptors and therefore reduces its own synthesis by inhibiting enzymes HMG-CoA reductase/synthase
25
Q

LDL receptors relation to high LDL

A
  • high LDL in the plasma correlates to atherosclerosis, because it saturates LDL receptors. Then, it enters via a nonspecific endocytic process leading to excessive cholesterol uptake
26
Q

what does “bulk-phase pinocytosis” refer to?

A

unregulated uptake of cholesterol because of excess LDL

27
Q

Beta-oxidation pathway

A

series of enzyme catalyzed rxns that degrade FA’s by removing 2-carbon units from the carboxyl end
- takes place in the mito matrix

28
Q

1st part of Beta-oxidation pathway

A

free FA’s need to be activated, which occurs by the enzyme fatty acyl-CoA synthetase. Turns free FA’s into fatty acyl-CoA
- occurs in the cytoplasm, requires ATP

29
Q

beta-oxidation pathway if FA chain is large

A

fatty acyl-CoA changes carriers from CoA to carnitine in the IMS, so that it can move into the mito matrix.
- changes back to CoA in the mito matrix

30
Q

beta-oxidation overview

A

highly exergonic, purpose it to generate energy through the break down of FA’s, needs 2 ATP
results in:
- 1 NADH
- 1 FADH2
- 1 acetyl-CoA and 1 fatty acyl-CoA

31
Q

what can the product of beta-oxidation (acetyl-CoA) be used for?

A

the citric acid cycle or becomes a ketone body

32
Q

ketone bodies use

A

important metabolic fuel for many peripheral tissues
- such as, heart and skeletal muscle, or the brain (uses ketone bodies as fuel in starvation)

33
Q

ketosis

A

a condition in which ketone bodies are produced faster than metabolized, leads to ketoacidosis (lowered blood pH)

34
Q

FA biosynthesis

A
  • occurs through condensation of C2 units, opposite of beta-oxidation (different pathway though)
  • mainly in the liver and adipose tissue
  • takes place in cytoplasm, endergonic process
35
Q

requirements for FA biosnythesis

A

each round requires:
- an activated malonyl-CoA (1 ATP per round for activation)
- 2 NADPH

36
Q

regulation of FA metabolism

A
  • glucagon, epinephrine, and norepinephrine stimulate cAMP, which stimulates PKA (phosphorylation)= active beta-oxidation and inhibited FA biosynthesis
  • insulin decreases cAMP, activates acetyl-CoA carboxylase (dephosphorylation) = active FA biosynthesis, inhibits beta-oxidation
37
Q

AMPK on FA metabolism

A
  • activated by AMP and inhibited by ATP
  • promotes catabolic process and inhibits anabolic ones (so activates glycolysis and FA oxidation, inhibits FA synthesis)

OPTOM 8060 BIOCHEM Midterm 2 (8 decks)

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